Healthy human joint surfaces are covered by articular cartilage, which provides a resilient, durable surface with low friction, for distribution of mechanical forces and protection of the underlying bone. Cartilage is an avascular tissue, having a small number of chondrocytes encapsulated within an extensive extracellular matrix. Damage to the articular cartilage, subchondral bone, or both can result from traumatic injury or a disease state.
There are significant differences in the ability of natural tissues to respond in vivo to different types of injury or disease. Injuries that do not penetrate subchondral bone are associated with a limited repair response. In contrast, osteochondral injuries in which the subchondral bone is penetrated can participate in a repair response due to the influx of reparative cells from the bone marrow. Formation of fibrocartilage, a mixture of hyaline cartilage and fibrous tissue, characterizes the repair response. Fibrocartilage lacks the durability or mechanical properties of normal articular cartilage, and eventually degrades from normal joint use. Many osteochondral injuries become clinically asymptomatic for a period of several years as a result of fibrocartilage formation. Secondary degeneration at the site of the injury can ultimately result in poor joint function, pain, and disability.
Osteochondral grafting has been used to repair or replace articular cartilage and the underlying bone. In osteochondral grafting, cartilage is harvested with the corresponding subchondral bone from a region of less strain, and the cartilage and bone tissue of the defect site is removed by milling, to create a bore of a precise geometry. The harvested tissue is then implanted into the defect site. Healing of the graft bone to the host bone results in fixation of the graft to the host. Larger defects are repaired with several bores, in a procedure termed mosaic plasty. The potential for donor site morbidity, produced by harvest of the autologous graft, however, presents a major remaining disadvantage. Further, potential donor site morbidity limits effective treatment of a defect to a greater extent as the size of the defect increases.
There continues to be a need for an osteochondral implant that can restore normal joint function, and that addresses the limitations of current osteochondral graft technology.